Galectin 2 regulates JAK/STAT3 signaling activity to modulate oral squamous cell carcinoma proliferation and migration in vitro
XINRU FENG1, LI XIAO2,*
1 Medical School, University of Electronic Science and Technology of China, Chengdu, 610072, China
2 Department of Stomatology, Sichuan Provincial People’s Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China
* Address correspondence to: Li Xiao, xiao1985621@163.com
(This article belongs to the Special Issue: Subcellular Organelles and Cellular Molecules: Localization, Detection, Prediction, and Diseases)
BIOCELL https://doi.org/10.32604/biocell.2024.048395
Received 06 December 2023; Accepted 18 February 2024; Published online 18 March 2024
Abstract
Background: Galectin 2 (LGALS2) is a protein previously reported to serve as a mediator of disease progression
in a range of cancers. The function of LGALS2 in oral squamous cell carcinoma (OSCC), however, has yet to be explored,
prompting the present study to address this literature gap.
Methods: Overall, 144 paired malignant tumor tissues and
paracancerous OSCC patient samples were harvested and the LGALS2 expression levels were examined through qPCR
and western immunoblotting. The LGALS2 coding sequence was introduced into the pcDNA3.0 vector, to enable the
overexpression of this gene, while an LGALS2-specific shRNA and corresponding controls were also obtained. The
functionality of LGALS2 as a regulator of the ability of OSCC cells to grow and undergo apoptotic death in vitro was
assessed through EdU uptake and CCK-8 assays, and flow cytometer, whereas a Transwell system was used to assess
migratory activity and invasivity. An agonist of the Janus Kinase 2 (JAK2)/Signal Transducer and Activator of
Transcription 3 (STAT3) pathway was also used to assess the role of this pathway in the context of LGALS2
signaling.
Results: Here, we found that lower LGALS2 protein and mRNA expression were evident in OSCC tumor
tissue samples, and these expression levels were associated with clinicopathological characteristics and patient survival
outcomes. Silencing LGALS2 enhanced proliferation in OSCC cells while rendering these cells better able to resist
apoptosis. The opposite was instead observed after LGALS2 was overexpressed. Mechanistically, the ability of LGALS2
to suppress the progression of OSCC was related to its ability to activate the JAK/STAT3 signaling axis.
Conclusion:
Those results suggest a role for LGALS2 as a suppressor of OSCC progression through its ability to modulate JAK/
STAT3 signaling, supporting the potential utility of LGALS2 as a target for efforts aimed at treating OSCC patients.
Keywords
LGALS2, Oral squamous cell carcinoma (OSCC), Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2-STAT3), Progression
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